SLC4A7 Drives NSCLC Progression and Immune Evasion via pH Dysregulation: Its Targeting Synergizes with Anti-PD-1/L1 Therapy
Abstract
data demonstrate that the alkalinization of the TME induced by Slc4a7 knockout enhances the infiltration and function of cytotoxic T cells, significantly inhibiting tumor growth. Additionally, Slc4a7 knockout exhibits synergistic antitumor efficacy in combination with PD-1/PD-L1 immune checkpoint inhibitors. Mechanistically, integrative analysis of RNA-seq and ATAC-seq data identified CTCF as a transcription factor regulating SLC4A7 expression. In summary, our study demonstrates that SLC4A7-mediated bicarbonate transport is crucial for maintaining acid-base homeostasis in NSCLC and represents a promising therapeutic target for this disease.
Fields of Study & Subjects
Amino Acid Enzymes and Metabolism
Ion Transport and Channel Regulation
Diabetes Treatment and Management
Publication details
- Journal / source
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Volume
- 22
- Issue
- 8
- Pages
- 3950–3968
- Publication date
- 30 March 2026
- Language
- EN